Clinical Study Temporal Bone Pneumatization and Pulsatile Tinnitus Caused by Sigmoid Sinus Diverticulum and/or Dehiscence
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1 BioMed Research International Volume 2015, Article ID , 4 pages Clinical Study Temporal Bone and Pulsatile Tinnitus Caused by Sigmoid Sinus Diverticulum and/or Dehiscence Liu Wenjuan, 1,2 Liu Zhaohui, 3 Zheng Ning, 2 Zhao Pengfei, 1 Dong Cheng, 1 and Wang Zhenchang 1 1 Department of Radiology, Beijing Friendship Hospital, Capital Medical University, Beijing , China 2 DepartmentofRadiology,JiningNo.1People shospital,shandong272002,china 3 Department of Radiology, Beijing Tongren Hospital, Capital Medical University, Beijing , China Correspondence should be addressed to Liu Zhaohui; lzhtrhos@163.com and Wang Zhenchang; cjr.wzhch@vip.163.com Received 3 March 2015; Accepted 21 April 2015 Academic Editor: Tobias Kleinjung Copyright 2015 Liu Wenjuan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Although air cells within temporal bone may play an important role in the transmission of pulsatile tinnitus (PT) noise, it has not been studied systematically. Purpose. To evaluate the difference in temporal bone pneumatization between PT patients with sigmoid sinus diverticulum and/or dehiscence (SSDD) and healthy people. Material and Methods. A total of 199 unilateral persistent PT patients with SSDD and 302 control subjects underwent dual-phase contrast-enhanced CT (DP-CECT), to assess the of temporal bone pneumatization in each ear. Results.In thebilateral temporal bone of 302 controls,16 ears were I,53 were II, 141 were III, and 394 were IV. Among the affected ears of 199 PT cases, 1 ear was I, 18 were II, 53 were III, and 127 were IV. There was no significant difference in the pneumatization between the affected PT ear and either ear in the healthy subjects (p > 0.05). Conclusion. Although air cells within the temporal bone are an important factor in the occurrence of PT, its severity does not differ significantly from the pneumatization of healthy people. 1. Introduction Tinnitus is a common otologic symptom affecting 30% of the population worldwide [1]. Approximately 4% of patients have pulsatile tinnitus (PT), defined as the perception of somatosounds synchronized with the pulse in the absence of an external acoustic stimulus [2]. The psychological impact of PT on many patients is so severe that it can lead to depression or even suicide [3]. Although PT has numerous causes, sigmoid sinus diverticulum and/or dehiscence (SSDD) is the most frequent and treatable cause [4 10]. Some studies report that SSDD is the cause of PT in up to 20% of cases [5, 8, 9]. The mechanism of PT caused by SSDD remains unclear. Many studies have suggested that sound in the sigmoid sinus or vibration of the sigmoid wall caused by blood flow is transmitted to the inner ear through the dehiscent sigmoid sinus plate and air cells within the temporal bone, which is ultimately sensed as PT [8, 10, 11]. Thus, the air cells within the temporal bone may be an important contributor to PT occurrence. However, the magnitude of temporal bone pneumatization necessary to trigger PT and the difference between PT patients and healthy people, which is critical to the etiological diagnosis and may affect therapeutic planning, is still debated at present. Some studies suggest that the diffused pneumatization in temporal bone and the pneumatization in patients with PT caused by the internal carotid artery (ICA) were greater than those observed in healthypeopleandmaybeanimportantcontributortopt. Sözen et al. [12] evaluated the relationship between subjective PT and petrous bone pneumatization by comparing 25 PT patients with healthy individuals. They detected petrous bone pneumatization in 22 (68.8%) of 32 ears with subjective PT, which was statistically higher than the prevalence in control subjects (24%). By contrast, a different study found that 80% of PT patients with sigmoid sinus diverticulum exhibited hyperpneumatization or good pneumatization of the temporal bone, while 20% of their patient sample exhibited moderate pneumatization of the temporal bone [11].
2 2 BioMed Research International The aim of this study was to evaluate the temporal bone pneumatization in PT caused by SSDD by comparing patients diagnosed with PT and healthy control subjects. We hypothesized that the temporal bone pneumatization of the PT group was greater than the pneumatization in the control subjects. 2. Materials and Methods 2.1. Subjects. The Hospital Institutional Review Board for HumanSubjectsResearchapprovedthisstudy.Weevaluated the pneumatization of temporal bone in the unilateral PT group and control group. The PT group included 199 SSDD patients comprising 18 male and 181 female diagnosed with unilateral PT between May 2008 and January Sixty-five patients had left PT, and 134 had right PT. The duration of PT was 3 months to 36 years. All patients were diagnosed with SSDD using dual-phase contrast-enhanced computed tomography (DP-CECT) of the temporal bone, and other causes of PT, which was proven by imaging examination and other clinical examination, such as aberrant internal carotid artery, abnormal emissary vein, dural arteriovenous fistula, benign intracranial hypertension, carotid atherosclerosis, paraganglioma, high-riding or dehiscent jugular bulb, or otosclerosis, were excluded. Thirty-eight patients suffering severe and continuous tinnitus underwent surgery of sinus wall reconstruction. Among them, the PT resolved completely in 29 patients and decreased significantly in the remaining 9 patients. Among 937 consecutive patients with orbital tumors, paranasal sinus tumors, or orbital trauma undergoing DP-CECT between May 2008 and January 2013 whodidnothaveahistoryoftinnitus,weidentified302 patients (209 male and 93 female) as controls after excluding patients undergoing brain surgery or those with low-quality images, temporal bone fracture, and other ear pathologies Imaging Method. DP-CECT was performed in all patients using a 64-slice multidetector CT (Brilliance 64; Philips, Best, Netherlands) at the following parameters: 120 kvp, 300 ma, detector collimation mm, rotation time 0.75 s, pitch 0.89 : 1, matrix , and field-ofview (FOV) 22 22cm.Thescanrangewasfromthevertex to the sixth cervical vertebrae. Iodinated nonionic contrast agent (Iopamidol (370 mg iodine/ml); Bracco, Shanghai, China) was administered at 5 ml/s using an electric power injector. The contrast agent was dosed at 1.5 ml/kg according to the patient s weight in all subjects. The ascending aorta served as the trigger point, the trigger area measured 200 mm 2, and the trigger threshold was set at 150 HU. The arterial phase was triggered by the Bolus-Tracking program (Trigger Bolus software; Philips, Best, Netherlands) after administering the contrast agent and performed in the cephalocaudal direction. The arterial phase time ranged from 8 to 12 s. The venous phase scan was performed in the opposite direction after a fixed 8 s delay. All arterial phaseimageswerereconstructedbystandardalgorithms,and standard and bone algorithms were used in all venous phase images Image Interpretation. The CT images were reviewed by two radiologists (LZH and LWJ, with 13 and 11 years of experience, resp.), and the findings were determined by consensus. SSDD was diagnosed according to the following previously described criteria: incomplete thin bone surrounding the sigmoid sinus and/or a diverticulum entering the mastoid bone [5, 6, 13]. The temporal bone pneumatization was classified according to the method described by Han et al. [14]. The sigmoid sinus was the designated reference for evaluation. On the image in which the malleoincudal complex resembled an ice cream cone-shape, three parallel lines angled 45 anterolaterally were applied so that one line crossed the most anterior point of the sigmoid sinus at its junction with the petrous bone, the second line crossed the most lateral margin along the transverse plane of the sigmoid groove, andthethirdlinecrossedthemostposteriorpointofthe sigmoid sinus, respectively. The magnitude of temporal bone pneumatization was classified into four categories as follows: I (hypopneumatization), the pneumatization remained anteromedial to the line drawn at the most anterior point of the sigmoid sinus; II (moderate pneumatization), the pneumatization extended into the space between the two lines at the most anterior and lateral aspects of the sigmoid sinus; III (good pneumatization), the pneumatization extended to the space between the two lines at the most lateral and posterior aspects of the sigmoid sinus; and IV (hyperpneumatization), the pneumatization extended posterolaterally beyond the line drawn at the most posterior pointofthesigmoidsinus Data Analysis and Statistics. All statistical analyses were performed using statistical software (SPSS, version 16.0; SPSS, Chicago, IL USA), and a p value less than 0.05 was considered statistically significant. The χ 2 test was used initially to analyze the control group according to laterality and gender. The independent t-test was then used to access the PT and control groups according to age. If there were no differences in the pneumatization between each lateral side and gender in the control group, and the patient ages could be matchedbetweenthetwogroups,thentheχ 2 test was used to analyze the proportional data between the affected side of the PT patients and the control subjects. 3. Results Tables 1 and 2 list the temporal bone pneumatization per lateral side and gender, respectively, in the control group. There was no significant difference according to laterality (p = 0.471) or gender (p = 0.775). The PT group included 199 PT patients with a mean age of 40.6±13.8 years (range years), and the control group included 302 patients with a mean age of 40.8 ± 11.7 years (range years). There was no significant difference in age between the PT and control groups (p = 0.865). As shown in Table 3, there was no significant difference in the pneumatization between the affected side in the PT group and either side in the control group (p = 0.263).
3 BioMed Research International 3 Table 1: Comparison of temporal bone pneumatization between left and right ears in control group. I 8 8 Side (number of ears) Statistical analysis Left Right χ 2 p II III IV Total Table 2: Comparison of temporal bone pneumatization by gender in control group. Gender (number of ears) Statistical analysis Male Female χ 2 p I 12 4 II III IV Total Table 3: Comparison of temporal bone pneumatization between the PT and control groups. Group (number of ears) Statistical analysis PT side Control χ 2 p I 1 16 II III IV Total PT: pulsatile tinnitus. 4. Discussion Ourstudyfoundthatthetemporalbonepneumatization inpatientswithptwasidenticaltotheinhealthy people. Additionally, although sigmoid plate dehiscence has been reported as a cause of PT, we found that it also occurs in some healthy people. Therefore, abnormal blood flow within the sigmoid sinus is the essential factor triggering PT. Only when abnormal sigmoid sinus perfusion, sigmoid plate dehiscence, and normal temporal bone pneumatization coexist will PT potentially occur. Approximately 90.5% of the temporal bone pneumatization lesions were s II and IV (good pneumatization and hyperpneumatization), which supports the theory that extensive temporal bone pneumatization favors sound transmission, as suggested by others. Large air cells increase the resonance of sound and serve as an amplifier. Increased transmission of normal perfusion sounds to the cochlea would lead to PT [15, 16]. However, 9.5% of temporal bone pneumatization in the patient population were s I andii(hypopneumatizationandmoderatepneumatization). Multiple small air cells in poorly pneumatized temporal bone do not augment the resonance of blood flow vibration in the sigmoid sinus. However, the transmission distance from the sigmoid sinus to the inner ear is shorter than in extensively pneumatized temporal bone and therefore may be sensed as PT. In our study, DP-CECT was used to examine the detailed anatomic structure and accurately diagnose PT caused by SSDD. DP-CECT includes arterial and venous phases and can demonstrate the status of vessels and temporal bones simultaneously in a single study. Krishnan et al. [17]suggested that DP-CECT can effectively detect arterial, venous, and inner ear causes of PT in a prospective study of 16 PT patients. Han et al. [14] classified the temporal bone pneumatization into s I IV based on the sigmoid sinus, which can be used to assess pneumatization with good feasibility. The methodusedasinglectimageandassessedthestructureof the sigmoid sinus, which was found to accurately represent pneumatization in the entire temporal bone. In our study, we chose this method to classify the temporal bone pneumatization because it was simple and practical for a large sample analysis. Notably, our study is a retrospective study, and the difference in temporal bone pneumatization was analyzed between PT patients and healthy subjects. However, the specific mechanism generating the air cells within the temporal bone in PT was not examined and warrants further experimental study. 5. Conclusion The magnitude of temporal bone pneumatization does not significantly differ between PT patients with SSDD and healthy people, which indicates that normal pneumatized temporal bone can potentially meet the criteria of SSDD required to induce PT. Disclosure Liu Wenjuan and Liu Zhaohui are co-first authors. Conflict of Interests The authors declare that there is no conflict of interests regarding the publication of this paper. Acknowledgments This work was supported by Grant nos and from the National Natural Science Foundation of China and Grant no. 13JL03 from Capital Medical University, China. References [1] A. J. Heller, Classification and epidemiology of tinnitus, Otolaryngologic Clinics of North America,vol.36,no.2,pp , 2003.
4 4 BioMed Research International [2] J. L. Stouffer and R. S. Tyler, Characterization of tinnitus by tinnitus patients, Speech and Hearing Disorders,vol. 55,no.3,pp ,1990. [3] S. Pridmore, G. Walter, and P. Friedland, Tinnitus and suicide: Recent cases on the public record give cause for reconsideration, Otolaryngology Head and Neck Surgery, vol.147,no.2, pp ,2012. [4] F. Signorelli, K. Mahla, and F. Turjman, Endovascular treatment of two concomitant causes of pulsatile tinnitus: sigmoid sinus stenosis and ipsilateral jugular bulb diverticulum. Case report and literature review, Acta Neurochirurgica,vol.154,no. 1,pp.89 92,2012. [5] D. J. Eisenman, Sinus wall reconstruction for sigmoid sinus diverticulum and dehiscence: a standardized surgical procedure for a range of radiographic findings, Otology and Neurotology, vol. 32, no. 7, pp , [6] D. E. Mattox and P. Hudgins, Algorithm for evaluation of pulsatile tinnitus, Acta Oto-Laryngologica, vol. 128, no. 4, pp , [7] A. K. Grewal, H. Y. Kim, R. H. Comstock III, F. Berkowitz, H. J. Kim, and A. K. Jay, Clinical presentation and imaging findings in patients with pulsatile tinnitus and sigmoid sinus diverticulum/dehiscence, Otology and Neurotology, vol. 35, no. 1, pp , [8] J.Xue,T.Li,X.Sun,andY.Liu, Focaldefectofmastoidbone shell in the region of the transverse-sigmoid junction: a new cause of pulsatile tinnitus, The Laryngology & Otology,vol.126,no.4,pp ,2012. [9] K. J. Otto, P. A. Hudgins, W. Abdelkafy, and D. E. Mattox, Sigmoid sinus diverticulum: a new surgical approach to the correction of pulsatile tinnitus, Otology and Neurotology, vol. 28,no.1,pp.48 53,2007. [10] G.-P. Wang, R. Zeng, Z.-H. Liu et al., Clinical characteristics of pulsatile tinnitus caused by sigmoid sinus diverticulum and wall dehiscence: a study of 54 patients, Acta Oto-Laryngologica, vol. 134, no. 1, pp. 7 13, [11] Z. Liu, C. Chen, Z. Wang et al., Sigmoid sinus diverticulum and pulsatile tinnitus: analysis of ct scans from 15 cases, Acta Radiologica,vol.54,no.7,pp ,2013. [12] E. Sözen, I. Çelebi,Y.O.Uçal,andB.U.Coşkun, Is there a relationship between subjective pulsatile tinnitus and petrous bone pneumatization? The Craniofacial Surgery,vol. 24, no. 2, pp , [13] B. F. Branstetter and J. L. Weissman, The radiologic evaluation of tinnitus, European Radiology,vol.16,no.12,pp , [14] S. J. Han, M. H. Song, J. Kim et al., Classification of temporal bone pneumatization based on sigmoid sinus using computed tomography, Clinical Radiology, vol.62,pp ,2007. [15] M. Tüz, H. Doğru, and A. Yeşildağ, Subjectivepulsatiletinnitus associated with extensive pneumatization of temporal bone, Auris Nasus Larynx,vol.30,no.2,pp ,2003. [16] O. Topal, S. S. Erbek, S. Erbek, and L. N. Ozluoglu, Subjective pulsatile tinnitus associated with extensive pneumatization of temporal bone, European Archives of Oto-Rhino-Laryngology, vol. 265, no. 1, pp , [17] A. Krishnan, D. E. Mattox, A. J. Fountain, and P. A. Hudgins, CT arteriography and venography in pulsatile tinnitus: preliminary results, The American Neuroradiology, vol.27, no. 8, pp , 2006.
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